Sugammadex is widely used for rapid and predictable reversal of aminosteroid neuromuscular blockade and has a favorable safety profile. However, rare cardiovascular adverse events, including severe hypotension, bradycardia, and asystole, have been reported. We describe a case of a 39-year-old healthy male who developed profound hypotension without bradycardia approximately six minutes after receiving sugammadex for reversal of moderate neuromuscular blockade following uncomplicated orthopedic surgery. His blood pressure decreased from 95/51 mmHg at baseline to 68/33 mmHg six minutes after sugammadex administration, reaching a nadir of 50/29 mmHg at 17 min, with a heart rate of 117 beats/min. The patient had stable intraoperative hemodynamics and no evidence of bronchospasm, cutaneous manifestations, or airway compromise at the time of the event. Hypotension was refractory to repeated boluses of phenylephrine and ephedrine, with subsequent improvement following norepinephrine administration. The patient recovered without further complications and was discharged the same day. Although causality cannot be definitively established, the temporal relationship raises concern for sugammadex-associated hypotension without bradycardia, possibly related to an atypical hypersensitivity reaction. This case highlights that severe hypotension may occur even in low-risk patients in the absence of bradycardia or other classic features of anaphylaxis, requiring prompt recognition and early potent vasopressor support.

Whether ephedrine, when used to maintain intraoperative blood pressure, is superior to phenylephrine in reducing postoperative delirium remains uncertain. This study aims to determine whether the intraoperative management of hypotension with ephedrine, compared with phenylephrine, reduces the incidence of postoperative delirium in elderly patients undergoing major non-cardiac, non-neurosurgical surgery.

Asthma affects 260-300 million people worldwide. About 20%-35% of patients use medicinal plants with their asthma medication, often without telling their clinicians. Disclosure rates are low; up to 42% of asthma outpatients use herbal products, with no records in their charts. Previous reviews discussed herb-drug interactions and asthma phytotherapy separately. There is no combined pharmacokinetic, pharmacodynamic, and toxicological evidence for all modern anti-asthma agents. This review closes that gap. It draws from mechanistic, preclinical, and clinical data. It looks at eight common botanicals: Glycyrrhiza glabra, Curcuma longa, Nigella sativa, Boswellia serrata, Tylophora indica, Adhatoda vasica, Astragalus membranaceus, and Piper nigrum. The review explains how these botanicals affect cytochrome P450 isoenzymes, Phase II conjugative enzymes, and membrane transporters, including P-glycoprotein. It also considers shared adrenergic, glucocorticoid-receptor, and inflammatory targets of inhaled corticosteroids, β2-agonists, leukotriene receptor antagonists, theophylline, and biologic agents. These interactions create clinical hazards. For example, Hypericum perforatum increases CYP3A4 activity by up to 11-fold and can destabilize theophylline and corticosteroid levels. Ephedra sinica causes dose-dependent sympathomimetic toxicity, which worsens β2-agonist cardiovascular risk. Glycyrrhiza glabra may trigger pseudoaldosteronism and hypokalaemia by inhibiting 11β-hydroxysteroid dehydrogenase type 2. Ginkgo biloba has been tied to bleeding events. Turmeric, previously seen as safe, now appears in drug-induced liver injury registries. Compositional variability adds to the risk; for example, hyperforin content can range from 0.01% to 1.89%, and ephedrine content varies by more than 12-fold across products. This review places its findings in the context of the WHO Global Traditional Medicine Strategy 2025-2034. It identifies important herb-anti-asthma drug pairs, defines monitoring endpoints, and proposes a pharmacogenetically informed framework for safely integrating medicinal plants into asthma care.

Methamphetamine (MA) is a widely abused illicit drug synthesized primarily using either ephedrine/pseudoephedrine or 1-phenyl-2-propanone (P2P) as precursors. These processes generate precursor-derived impurities that can provide valuable forensic intelligence. However, recent advances in purification techniques have resulted in refined MA samples containing impurities at ultra-trace levels, thereby posing analytical challenges for conventional gas chromatography-based methods. In this study, a highly sensitive liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was developed for the targeted detection of MA precursor-associated impurities at ultra-trace levels. A total of 19 impurities, including markers associated with the P2P and ephedrine/pseudoephedrine precursor classes, were analyzed using multiple reaction monitoring (MRM) mode. Chromatographic and mass spectrometric conditions were optimized to achieve high sensitivity and selectivity. The developed method demonstrated limits of detection ranging from 0.008 to 2.500 ng/mg and showed satisfactory selectivity and repeatability for qualitative identification. The method was applied to 33 high-purity seized MA samples to evaluate precursor-associated impurity profiles and regional differences based on documented geographical origins. Differences in impurity patterns were observed between samples from North America and Southeast Asia, reflecting regional variation in these profiles. P2P-related impurities were detected in North American samples, whereas Southeast Asian samples exhibited more variable profiles, including both P2P- and ephedrine/pseudoephedrine-related markers. These results demonstrate that the proposed LC-MS/MS method enables reliable detection of ultra-trace level impurities and provides a valuable analytical tool for impurity profiling and forensic intelligence applications, particularly for highly purified MA samples.

Substance exposure among pediatric emergency department (ED) patients may be underrecognized because routine urine immunoassays have limited analytical sensitivity, and objective confirmatory toxicological data in pediatric ED populations remain limited.

Spinal anaesthesia is the most commonly used anaesthetic technique for caesarean section due to its rapid onset, reliability, and favourable safety profile. Despite these advantages, spinal-induced hypotension remains a common complication with potential adverse effects on maternal and fetal well-being, including nausea, vomiting, dizziness, reduced cardiac output, and impaired uteroplacental perfusion. Phenylephrine remains the guideline-supported first-line vasopressor for spinal-induced hypotension during caesarean delivery because of its effectiveness in maintaining maternal blood pressure and its favourable fetal acid-base profile, including a lower risk of fetal acidosis compared with ephedrine. However, it may cause reflex bradycardia and reduced maternal cardiac output. Norepinephrine (noradrenaline) has emerged as a promising alternative because its α-adrenergic effects, combined with modest β1 activity, may better preserve maternal heart rate and cardiac output. A narrative literature review was conducted using PubMed/MEDLINE, Scopus, and Google Scholar. Studies were included if they evaluated maternal haemodynamic outcomes, adverse maternal effects, neonatal outcomes, or vasopressor efficacy during caesarean delivery under spinal anaesthesia. Recent trials and meta-analyses suggest that noradrenaline provides comparable efficacy to phenylephrine, with similar neonatal outcomes and potential maternal haemodynamic advantages. However, phenylephrine remains the current guideline-supported first-line agent, while noradrenaline requires further clarification regarding optimal dosing, safety, and routine first-line use. This review evaluates phenylephrine and noradrenaline for both prophylaxis and rescue treatment of spinal-induced hypotension during caesarean section.

Background/Objectives: Intraoperative hypotension (IOHs) affects up to 87% of patients under general anesthesia and is consistently associated with acute kidney injury, myocardial damage, stroke, and mortality. The intermittent unavailability of ephedrine across healthcare systems underscores the need for evidence-based alternatives. This review critically evaluates pharmacological options for IOH when ephedrine is unavailable, focusing on receptor pharmacodynamics, population-specific evidence, and clinical consequences of inadequately managed hypotension. Methods: A narrative, evidence-based review was conducted examining mechanisms of action, dosing strategies, adverse effect profiles, and clinical applicability of key vasoactive agents: ephedrine, phenylephrine, norepinephrine, and epinephrine. Population-specific evidence across obstetric, pediatric, and elderly cohorts was synthesized from randomized controlled trials, meta-analyses, and observational studies. The clinical impact of IOH on neurological, cardiovascular, and renal outcomes was reviewed. Results: Each vasopressor exhibits a distinct receptor-selectivity profile that determines its hemodynamic effect and optimal clinical context. Norepinephrine's favorable α1/β1 balance tends to preserve cardiac output better than pure α1-agonists and has emerged as a promising alternative in obstetric and elderly populations, although the optimal agent ultimately depends on the underlying mechanism of hypotension and individual patient characteristics. Epinephrine provides combined vasopressor and inotropic support for hypotension with myocardial depression. IOH is associated with a greater than twofold increase in postoperative AKI and significantly elevated risks of myocardial infarction and stroke, with outcomes driven by cumulative hypotensive exposure rather than isolated pressure nadirs. Conclusions: Effective management of IOH requires individualized vasopressor selection guided by underlying pathophysiology, cardiovascular profile, and surgical context. A physiology-based strategy-rather than protocol-driven drug substitution-enables anesthesiologists to achieve precise hemodynamic control and preserve end-organ perfusion even when ephedrine is unavailable.